LEFT-VENTRICULAR FUNCTION AND PROGNOSIS AFTER MYOCARDIAL-INFARCTION -RATIONALE FOR THERAPEUTIC STRATEGIES

Citation
R. Scognamiglio et al., LEFT-VENTRICULAR FUNCTION AND PROGNOSIS AFTER MYOCARDIAL-INFARCTION -RATIONALE FOR THERAPEUTIC STRATEGIES, Cardiovascular drugs and therapy, 8, 1994, pp. 319-325
Citations number
45
Categorie Soggetti
Pharmacology & Pharmacy","Cardiac & Cardiovascular System
ISSN journal
09203206
Volume
8
Year of publication
1994
Supplement
2
Pages
319 - 325
Database
ISI
SICI code
0920-3206(1994)8:<319:LFAPAM>2.0.ZU;2-Z
Abstract
Prognosis after acute myocardial infarction is strongly associated wit h left ventricular dysfunction. However, asynergy does not necessarily imply loss of viability and myocardial necrosis. In fact, two differe nt patterns of contractile dysfunction, possibly coexisting, have been shown after acute myocardial infarction: Stunning and hibernation rep resent distinct patterns of contractile dysfunction that share the cha racter of reversibility. It is noteworthy, then, to identify the prese nce of these two conditions at the bedside and to develop medical trea tment to effect recovery of myocardial dysfunction. This strategy has the potential to ameliorate the outcome of patients after acute myocar dial infarction by improving left ventricular function. Beta-blocker t herapy significantly reduces mortality and the incidence of reinfarcti on after an acute myocardial infarction: These benefits result from th e prevention of sudden death, the reduction of the extent of myocardia l injury during the acute phase, and a further antiischemic action. Ne vertheless, beta-blocker therapy increases left ventricular dilatation . Recent experimental and clinical data show that ACE inhibitors confe r positive therapeutic effects after myocardial infarction by reducing the extent of left ventricular dilation, by reducing mortality, and b y improving the clinical outcome. Not all patients, however, can be su bjected to this therapeutical approach because of the possible detrime ntal effects produced by hypotension and by block of neurohormonal act ivation, sometimes truly compensatory in the early phase. Therefore, i t would be interesting to suggest a combination therapy of a beta-bloc ker with a vasodilator agent (ACE inhibitor or calcium channel blocker ).